The Journal of Experimental Medicine
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© The Rockefeller University Press, 0022-1007/1997/2/491/ $5.00
The Journal of Experimental Medicine, Volume 185, Number 3, February 3, 1997 491-498

Articles

Involvement of Egr-1/RelA Synergy in Distinguishing T Cell Activation from Tumor Necrosis Factor-{alpha}–induced NF-{kappa}B1 Transcription

Patricia C. Cogswell*, Marty W. Mayo*, and Albert S. Baldwin, Jr.*,{ddagger}

From the * Lineberger Comprehensive Cancer Center, and {ddagger} Department of Biology, University of North Carolina, Chapel Hill, North Carolina 27599-7295

NF-{kappa}B is an important transcription factor required for T cell proliferation and other immunological functions. The NF-{kappa}B1 gene encodes a 105-kD protein that is the precursor of the p50 component of NF-{kappa}B. Previously, we and others have demonstrated that NF-{kappa}B regulates the NF-{kappa}B1 gene. In this manuscript we have investigated the molecular mechanisms by which T cell lines stimulated with phorbol 12-myristate 13-acetate (PMA) and phytohemagglutin (PHA) display significantly higher levels of NF-{kappa}B1 encoding transcripts than cells stimulated with tumor necrosis factor-{alpha}, despite the fact that both stimuli activate NF-{kappa}B. Characterization of the NF-{kappa}B1 promoter identified an Egr-1 site which was found to be essential for both the PMA/ PHA-mediated induction as well as the synergistic activation observed after the expression of the RelA subunit of NF-{kappa}B and Egr-1. Furthermore, Egr-1 induction was required for endogenous NF-{kappa}B1 gene expression, since PMA/PHA-stimulated T cell lines expressing antisense Egr-1 RNA were inhibited in their ability to upregulate NF-{kappa}B1 transcription. Our studies indicate that transcriptional synergy mediated by activation of both Egr-1 and NF-{kappa}B may have important ramifications in T cell development by upregulating NF-{kappa}B1 gene expression.

Address correspondence to Albert S. Baldwin, Lineberger Comprehensive Cancer Center, Campus Box No. 7295, University of North Carolina, Chapel Hill, NC 27599.

This work was funded by the National Institute of Health (NIH) grant AI35098 awarded to A.S Baldwin and by the NIH postdoctoral fellowship grant 1F32-CA69790-01 awarded to M.W. Mayo.

1Abbreviations used in this paper: Egr-1; early growth response gene product; EMSA, electrophoretic mobility shift assay.

P.C. Cogswell and M.W. Mayo contributed equally to the scientific merit and preparation of this manuscript.


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